The Role of Mitochondria in Diabetic Kidney Disease

Stein Hallan, Kumar Sharma

Research output: Contribution to journalReview article

31 Scopus citations

Abstract

Despite major improvements in the treatment of patients with diabetes mellitus, many patients still suffer from progressive diabetic kidney disease. More research is needed to improve treatment and to understand why some patients develop complications while others do not. Mitochondrial dysfunction has turned out to be central to the pathogenesis of diabetes, and we will review some new aspects in this field and the potential for treatment. The conventional theory has been that the intracellular surplus of glucose leads to mitochondrial overproduction of superoxide that contributes to general cell damage and activation of deleterious pathways specific for diabetes complications. However, recent data suggests that reduced mitochondrial activity could be the basis for disease progression and complications through increased inflammation and pro-fibrotic factors. Physical exercise is a very strong stimulus to mitochondrial biogenesis, and we now understand many of the underlying signaling pathways. Clinical trials have also shown that training, especially high-intensity training, can delay the onset of diabetes and improve insulin resistance. Furthermore, intermittent fasting and various pharmacological agents are other potential options for stimulating mitochondrial function and reducing the risk of development and progression of diabetic kidney disease.

Original languageEnglish (US)
Article number61
JournalCurrent Diabetes Reports
Volume16
Issue number7
DOIs
StatePublished - Jul 1 2016
Externally publishedYes

Keywords

  • Complications
  • Diabetes mellitus
  • Exercise
  • Kidney disease
  • Mitochondria
  • Pathogenesis

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Fingerprint Dive into the research topics of 'The Role of Mitochondria in Diabetic Kidney Disease'. Together they form a unique fingerprint.

  • Cite this